Search PubMed⌕ Search

Biomedical subjects

W Terres

Publications and source records attributed to W Terres.

At least 37 records · Page 2Linked to original sources
PubMed1996

Recombinant hirudin as a periprocedural antithrombotic in coronary angioplasty for unstable angina pectoris.

Percutaneous transluminal coronary angioplasty is often complicated by thrombotic abrupt vessel closure in patients with unstable angina pectoris. The present multicentre trial was performed to determine the feasibility of two-dose regimens of recombinant hirudin (r-hirudin) compared to standard heparin in patients undergoing coronary angioplasty for unstable angina, and to investigate the effects of the different treatment regimen on markers of coagulation activation. At five participating centres, 61 patients were randomly enrolled in one of two sequential groups of r-hirudin (group 1: 0.3 mg.kg-1 i.v. bolus, 0.12 mg.kg-1.h-1 i.v. infusion; 21 patients; group 2: 0.5 mg.kg-1 i.v. bolus, 0.24 mg.kg-1.h-1 i.v. infusion; 19 patients) or in a heparin control group (150 IU.kg-1 i.v. bolus, 20 IU.kg-1.h-1 i.v. infusion; 21 patients). Antithrombotic therapy was started immediately before coronary angioplasty and continued for 24 h. This was followed by a low-dose anticoagulant infusion for another 24 h (r-hirudin: 0.04 mg . kg-1 . h-1; heparin: 7 IU . kg-1 . h-1). Activated partial thromboplastin time, r-hirudin plasma concentrations by both immunological and functional assay, thrombin-hirudin complex, thrombin-antithrombin III complex, soluble fibrin, and prothrombin fragment 1 + 2 were closely monitored. The median partial thromboplastin time prolongations at 24 h vs baseline were found to be 1.9-fold and 2.3-fold in r-hirudin group 1 and dose group 2, respectively, and 3.0-fold in the heparin group. There was a dose-dependent correlation between partial thromboplastin time and the r-hirudin plasma levels (r = 0.61). In five of 21 patients of dose group 1, three of 19 patients of dose group 2, and 10/21 patients of the heparin group, partial thromboplastin time values exceeding the predefined target range prompted an interruption of the infusion. One major bleeding complication occurred in dose group 2. The functional assay for the estimation of r-hirudin plasma concentrations showed excellent correlations to the immunological technique (r = 0.99). Differences between the thrombin-hirudin complex levels could not be observed. Increased concentrations of thrombin-antithrombin III complex, soluble fibrin, and prothrombin fragment 1 + 2 were seen 4-8 h after coronary angioplasty and after reduction of the high-dose therapy in dose group 1 when compared with dose group 2 and the heparin group, respectively. Based on coagulation tests the present study showed the feasibility of a periprocedural antithrombotic regimen with r-hirudin for patients undergoing coronary angioplasty for unstable angina. In addition to the partial thromboplastin time the determination of r-hirudin plasma levels by a chromogenic substrate assay considerably improves the monitoring of therapy. The lower dose r-hirudin regimen seems to be suboptimal as periprocedural anticoagulation in coronary angioplasty patients as indicated by markers of thrombin generation and thrombin activity.

Adult↗
PubMed1996

-New aspects in antithrombotic therapy--platelet inhibitors-.

The aim of platelet inhibitory therapy in cardiology is to prevent undesired thrombus formation and, thus, to prevent complications of cardiovascular diseases. In Germany, 5 substances are approved for antiplatelet therapy. Acetylsalicylic acid, an inhibitor of platelet cyclooxygenase, has been shown to be effective at both high and low doses in the secondary prevention of myocardial infarction, coronary heart disease, and cerebrovascular disease. In addition, acetylsalicylic acid is effective in reducing the complications of unstable angina pectoris and coronary angioplasty, and in reducing the occlusion rate of aortocoronary bypass grafts. The addition of dipyridamole to acetylsalicylic acid has not been shown to result in any additional benefit in many clinical studies. Ticlopidine, an antagonist of ADP-induced platelet aggregation has been similarly effective as acetylsalicylic acid in the treatment of coronary heart disease. The principal side effect of the drug, the occurrence of neutropenia in about 1% of treated patients, makes regular blood cell counts mandatory during treatment. In the secondary prevention of cerebrovascular disease, the drug may be superior to acetylsalicylic acid. Trapidil is an anti-platelet substance which acts on platelets through various mechanisms including inhibition of the release of "platelet derived growth factor". In 3 smaller randomized studies, trapidil has been found to reduce the restenosis rate after coronary angioplasty. Abciximab, the Fab-fragment of an antibody against the platelet fibrinogen receptor glycoprotein 11b/IIIa has been shown to be effective in the prevention of acute and long-term complications of high-risk coronary angioplasty.

Blood Flow Velocity↗
PubMed1996

[Initial clinical and angiographic results with the AVE Micro-Stent].

UNLABELLED: The AVE Micro Stent is a flexible stent with a small surface. Aim of this study was to investigate safety and efficacy of this stent. 105 AVE Micro Stents were deployed in 78 lesions in 64 patients. The implantation was performed electively (19%), after unsatisfactory PTCA (59%), and as "bailout" (23%) into left main (1), LAD (23), LCX (15), RCA (19) or CABG (6). Minimal lumen diameter and percent diameter stenosis were measured by quantitative coronary angiography before and after interventions and, in 21 patients, after 3 months. Stent-implantation was successful in 62 of 64 patients. The passage of the AVE Micro Stents through deployed stents (46) was successful in all of 28 cases. There were no deaths or myocardial infarctions. In two patients, subacute thromboses with subsequent increase of CK occurred, which were successfully treated. The minimal lumen diameter was 0.77 +/- 0.62 mm before intervention, 2.98 +/- 0.48 mm after implantation (p < 0.001), and 2.03 +/- 1.21 after 3 months (p < 0.001). The percent diameter stenosis was 75 +/- 20% before intervention, 39 +/- 20% after PTCA and 0 +/- 12% after implantation (p < 0.001). After 3 months, six of 21 patients (29%) with follow-up angiography had a restenosis, defined as > 50% diameter stenosis compared with the reference vessel. CONCLUSIONS: 1) The AVE Micro Stent is a flexible stent, which can be safely and efficiently deployed even through implanted stents. 2) The AVE Micro Stent appears to be particularly suitable for "bailout" therapy of dissections. 3) The rate of subacute thrombosis was low with this stent.

Adult↗
PubMed1996

[Thrombus age as a determinant of lysis efficacy of in vitro produced platelet-fibrin thrombi].

Thrombus age as a determinant of lysis efficacy has rarely been investigated. We developed an in vitro model to study the lysis of collagen induced platelet-fibrin-thrombi of different ages. Histologically, the thrombi were similar to those found in coronary vessels of patients deceased from acute myocardial infarction or unstable angina. After 10 (TA10), 30(TA30) und 60 (TA60) min of thrombus aging thrombolysis over 30 min with urokinase alone or in combination with prostaglandin E1 was started. The efficacy of lysis with urokinase alone decreased with increasing thrombus age. After 30 min of lysis with urokinase alone weight of TA10-thrombi was reduced by 16.4 +/- 1.2 mg, of TA30-thrombi by 11.5 +/- 0.9 mg (p < 0.001 vs TA10-thrombi) and of TA60-thrombi by 7.8 +/- 1.1 mg (p < 0.001 vs TA30, p < 0.0001 vs TA10-thrombi). The addition of prostaglandin Ei augmented lysis of TA10-thrombi, after 30 min of lysis thrombus weight was reduced by 17.3 +/- 1.2 mg (p < 0.01 vs urokinase alone). Lysis of 30 and 60 min old thrombi was nearly unaffected. Thus, thrombus age is a strong predictor of lysis efficacy of in vitro collagen induced platelet-fibrin-thrombi.

Adult↗
PubMed1995

[Preliminary clinical results with intracoronary ultrasound angioplasty].

UNLABELLED: BASIS AND AIM OF STUDY: Low-frequency, high-intensity ultrasound has been shown, both in vivo and in vitro, selectively to remove arteriosclerotic plaques and thrombi. This study was undertaken to investigate the safety and effectiveness of intracoronary ultrasound angioplasty. PATIENTS AND METHODS: Ultrasound coronary angioplasty (UCA) with highly flexible ultrasound catheters (1.2 mm or 1.7 mm probe tip) was performed in 50 patients (36 men, 14 women; mean age 64.7 [33-79] years) with coronary heart disease involving one (n = 26 or several (n = 24) vessels. Indications for treatment were exercise-induced (n = 35) or unstable (n = 14) angina or acute myocardial infarction (n = 11). Treated lesions were in the anterior interventricular branch (n = 25), circumflex branch of the left coronary artery (n = 3) and right coronary artery (n = 22). 19 vessels were occluded, 24 lesions were partially thrombosed, 19 were calcified. 22 stenoses were longer than 20 mm. According to AHA/ACC criteria, 10 type A, 17 type B1, 6 type B2 and 17 type C lesions were treated. RESULTS: Total ultrasound time was 336 +/- 308 s; mean passing time through the stenosis was 233 +/- 289 (10-556) s. 17 of 19 occlusions were recanalised after 285 +/- 224 s. Percutaneous transluminal angioplasty (PTCA) was subsequently performed in 49 patients. The mean stenosis grade was reduced by UCA from initially 82 +/- 3 to 64 +/- 2% and by subsequent PTCA to 38 +/- 1%. Average flow grade rose from 1.5 to 1.9 after UCA and to 2.8 after PTCA. No vasospasm, atrioventricular block or perforation was caused by UCA. Angiography demonstrated dissection after PTCA in seven patients, treated in two with a stent. Both UCA and PTCA failed to achieve recanalization in one patient with a thrombotic occluded coronary artery after acute myocardial infarction. In all other patients there were no complications. CONCLUSION: The results show UCA to be a safe method for removing high-degree coronary artery stenosis or recanalize thrombotic occlusions.

Adult↗
PubMed1995

Rapid angiographic progression of coronary artery disease in patients with elevated lipoprotein(a)

BACKGROUND: The mechanisms underlying rapid angiographic progression of coronary artery disease are still unknown. Intravascular thrombosis with or without plaque rupture may be involved. METHODS AND RESULTS: In a prospective study in 79 patients with coronary artery disease and at least one coronary diameter stenosis > or = 50%, possible risk factors for rapid progression were investigated. Quantitative coronary angiography was performed twice at a mean time interval of 66 +/- 25 days. Rapid progression of coronary disease defined as (1) an increase > 10% in stenosis severity in at least one stenosis > or = 50%, (2) occurrence of a new stenosis > or = 50%, or (3) occlusion of a formerly patent vessel was found in 21 patients (27%). Between patients with rapid progression and those without, there were no significant differences in sex distribution, age, smoking history, frequency of hypertension or diabetes mellitus, and serum LDL cholesterol, HDL cholesterol, and apolipoprotein B concentrations. In contrast, serum lipoprotein(a) [Lp(a)] concentrations > or = 25 mg/dL were found in 14 of 21 patients (67%) with rapid progression of coronary artery disease but in only 19 of 58 (33%) in the group without progression (P = .007). The respective median Lp(a) concentrations were 66 mg/dL (range, 2 to 139) and 13 mg/dL (range, 2 to 211; P = .01). CONCLUSIONS: Lp(a) appears to be a risk factor for the rapid angiographic progression of coronary artery disease. The pathophysiological link between Lp(a) and rapid progression may be an interference with thrombolysis through the partial structural homology of Lp(a) with plasminogen.

Blood Pressure↗
PubMed1995

Endogenous tissue plasminogen activator and platelet reactivity as risk factors for reocclusion after recanalization of chronic total coronary occlusions.

A prospective study was performed to investigate the role of the endogenous fibrinolytic system and platelet function for the occurrence of reocclusion after successful recanalization of chronic coronary occlusions. At control coronary angiography 8 +/- 2 weeks after recanalization, reocclusion was found in 10 (21%) of 47 patients. After correction for angiographic and clinical confounding factors, endogenous concentrations of tissue plasminogen activator (TPA) were lower in patients with reocclusion than in patients without. In contrast, plasma levels of plasminogen activator inhibitor-1 and alpha 2-antiplasmin were similar in the two groups. The mean platelet volume was significantly higher in patients with reocclusion than in patients without. In addition, agonist-induced platelet aggregation in platelet-rich plasma was enhanced in the patients with reocclusion. Decreased endogenous plasma TPA concentrations and enhanced platelet reactivity may contribute to the occurrence of reocclusion after primarily successful coronary artery recanalization.

Aged↗
PubMed1995

Multicenter evaluation of the Strecker tantalum stent for acute coronary occlusion after angioplasty.

The Strecker stent is a balloon-expandable, flexible endoprosthesis constructed of knitted tantalum wire and has been implanted successfully in peripheral arteries. This study presents the first multicenter experience with implantation of this radiopaque device in the coronary arteries in 64 patients of 6591 consecutive percutaneous transluminal coronary balloon angioplasty (PTCA) procedures complicated by abrupt closure. In all except 1 patient the stents (n = 72) were correctly placed, and flow could be reestablished immediately. During hospitalization 12 (19%) patients had stent closures; 5 (8%) patients had Q-wave myocardial infarctions; and 13 (20%) patients underwent bypass surgery (4 on an emergency basis). The in-hospital mortality was 9%: 2 patients died after thrombotic stent occlusions; 2 patients had fatal bleeding complications; and 2 patients died after bypass surgery. Major bleeding complications at the puncture site were observed in 8 (12.5%) patients. Angiograms (n = 45) after 17 +/- 5 weeks revealed a stent patency rate of 89%. Thus the Strecker coronary stent proved to be helpful in the management of acute vessel closure during PTCA. However, in this first series a high incidence of early thrombotic occlusions and bleeding complications warrants close anticoagulation monitoring and limits broader indications.

Angioplasty, Balloon, Coronary↗
PubMed1995

Recombinant hirudin (HBW 023) prevents troponin T release after coronary angioplasty in patients with unstable angina.

OBJECTIVES: This study was performed to evaluate the efficacy of peri-interventional treatment with recombinant hirudin (r-hirudin [HBW 023]) compared with heparin in the prevention of troponin T release in patients with unstable angina. BACKGROUND: Percutaneous transluminal coronary angioplasty in patients with unstable angina is associated with a high risk of acute thrombotic complications. METHODS: Serial troponin T measurements were performed in 61 patients with unstable angina during the 48-h observation period after coronary angioplasty of the ischemia-related lesion. Patients were randomly assigned to peri-interventional intravenous treatment with either r-hirudin (dosage group I: 0.3-mg/kg body weight bolus, 0.12 mg/kg per h for 24 h; dosage group II: 0.5-mg/kg bolus, 0.24 mg/kg per h for 24 h) or heparin (150-IU/kg bolus, 20 IU/kg per h for 24 h). All patients received acetylsalicylic acid before coronary angiography. After 24 h, patients received a constant low dose infusion of either hirudin (0.04 mg/kg per h) or heparin (7 IU/kg per h) for another 24 h. The power of the study to detect a decrease in abnormal troponin T levels from 60% (heparin group) to 20% (combined r-hirudin groups) was 88%. RESULTS: Serial troponin T measurements revealed two peaks within the 48 h after coronary angioplasty in the heparin but not the hirudin groups. An elevated serum troponin T concentration (> 0.2 ng/ml) within 48 h of coronary angioplasty was found in 9 (24%) of 38 patients in the hirudin groups (5 [25%] of 20 in dosage group I; 4 [22%] of 18 in dosage group II) compared with 11 (58%) of 19 in the heparin group (p = 0.01). We observed major cardiac events (death, myocardial infarction, abrupt vessel closure) in 1 (4.8%) of 21 patients in dosage group I, 1 (5.3%) of 19 in dosage group II and 3 (14.3%) of 21 in the heparin group (p = 0.33). CONCLUSIONS: In this pilot trial, hirudin appears to be superior to heparin in preventing troponin T release after coronary angioplasty.

Angina, Unstable↗
PubMed1994

In vitro model to test the thrombogenicity of coronary stents.

Thrombotic occlusion is a major complication limiting the application of stents in coronary arteries. In an in vitro model we investigated the thrombogenicity of different stent materials and several medical regimens to prevent thrombotic occlusion. Experiments were conducted in a closed system of silicon tubing with circulating citrated platelet rich plasma of healthy volunteers (n = 7) and of patients (n = 7 for each condition). Patients were either treated with phenprocoumon or with high or low dose heparin in combination with aspirin alone (100 mg) or aspirin (990 mg) plus dipyridamole (225 mg). After placement of tantalum wire stents into the system platelet aggregates were visible after 13.5 +/- 3.0 min, and occlusion occurred after 15.0 +/- 3.5 min. Similarly, with implanted stainless steel stents aggregation was seen after 13.0 +/- 3.5 min and thrombosis occurred after 14.5 +/- 3.5 min (p < 0.001 vs control without stent). Microscopic examination revealed combined platelet fibrin thrombi occluding the lumen. Platelet components predominately covered stent wires, particularly at crossing points. In all experiments high-dose heparin prevented platelet aggregate formation and stent occlusion independently of additional aspirin or aspirin plus dipyridamole; perfusion time > 60 min (p < 0.001 vs no heparin). Low-dose heparin could not prevent clotting. With aspirin alone aggregates were visible after 16.0 +/- 4.0 min and clotting occurred after 23.0 +/- 5.0 min. In combination with dipyridamole aggregates were visible after 15.5 +/- 5.0 min and clotting after 21.0 +/- 4.0 min (NS vs aspirin alone). Phenprocoumon prevented platelet aggregate formation and stent occlusion; perfusion time > 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[Reopening of completely closed aortocoronary venous bypasses using angioplasty and 24-hour local fibrinolysis].

Recent occlusion of aortocoronary venous bypass grafts had occurred in three patients, aged between 64 and 67 years. In all three recanalization was achieved after 8 hours, two and five days, respectively, of coronary angioplasty combined with local urokinase infusion for 24 hours. The procedure consisted of passing a guide-wire through the occluded bypass graft, the tip of the wire then being advanced to the periphery of the native coronary artery. The balloon was then repeatedly dilated along the length of the graft. Primary opening was not achieved in one of the grafts, and the other two closed again, despite repeated and prolonged balloon dilatation. In all three patients a coronary infusion catheter was then placed into the graft lumen and urokinase (3 mill. units) infused over 24 hours. An angiogram 24 hours later demonstrated an open bypass graft (residual stenosis < 50%). Angiography 9 to 14 weeks later revealed restenosis in one case, but it was reopened by balloon dilatation and stent insertion, while the other two had remained open without significant stenosis.

Aged↗
PubMed1994

[One session diagnostic heart catheterization and balloon dilatation ("prima vista"-PTCA): results and risks].

Percutaneous transluminal coronary angioplasty (PTCA) immediately after elective diagnostic cardiac catheterization ("prima vista"-PTCA) was performed in 124 patients (group 1) with typical angina pectoris (96 men, 28 women; mean age 60 +/- 10 [25-86] years). In a case-control analysis the results and complications, as well as the volume of contrast media and amount of radiation exposure were compared with a group of patients with similar symptoms (group 2) who during the same period had undergone angiography at another hospital and subsequently PTCA in our department (96 men, 28 women; mean age 60 +/- 8 [39-78] years). The success rate in group 1 (122 of 138 stenoses: 92.1%) was similar to that in group 2 (122 of 138 stenoses: 88.4%). Complications (coronary artery dissection with occlusion, emergency operation, myocardial infarction) were rare in both groups (8 vs 5; difference not significant). But the combined procedure (group 1) used lower volumes of contrast medium (341 +/- 131 vs 250 +/- 113 ml; P < 0.001) and the cumulative fluoroscopic time was lower (33.7 +/- 19.5 vs 26.5 +/- 12.4 min; P < 0.002). With optimal logistic conditions, "prima vista"-PTCA under elective circumstances is a useful and patient-friendly alternative to the conventional two-session diagnostic and therapeutic procedures.

Adult↗
PubMed1994

Improved global and regional left ventricular function after angioplasty for chronic coronary occlusion.

Percutaneous transluminal coronary angioplasty can be performed safely and effectively in patients with chronic total coronary occlusion. To investigate the effect on left ventricular function, global and regional left ventricular ejection fraction were analyzed by contrast angiography in 49 patients before and 10 +/- 6 weeks after successful recanalization. Coronary angiography at follow-up showed reocclusion in 12 patients (24%). In 37 patients with patent arteries global ejection fraction increased from 55.8 +/- 7.1% at baseline to 62.5 +/- 11.3% at follow-up (P < 0.001), and regional wall motion assessed by the centerline method improved from -1.7 +/- 1.0 to -0.6 +/- 1.5 standard deviations/chord (P < 0.001). In contrast, in patients with reocclusion neither global ejection fraction nor regional wall motion were significantly different at follow-up compared with baseline. Changes in global or regional left ventricular function after coronary recanalization were unrelated to other parameters such as severity of angina, duration of occlusion, history of myocardial infarction, presence or absence of visible collaterals, or baseline left ventricular function. Thus in patients with primarily successful recanalization of chronically occluded coronary arteries persistent vessel patency is the major determinant of global and regional improvement of left ventricular function.

Adult↗
PubMed1994

Changes in cardiovascular risk profile during the cessation of smoking.

The present study evaluated the intraindividual changes of serum lipids, blood pressure, adrenergic stimulation, and platelet reactivity in chronic smokers undergoing controlled smoking cessation assisted by nicotine chewing gum. One hundred twenty-one healthy smokers, who had smoked at least 20 cigarettes a day for at least 5 years, were included in the study. Serum lipids, blood pressure, catecholamine concentrations in serum and urine, platelet volume and platelet function in vitro were assessed during an initial phase of continued smoking, after stopping smoking during nicotine gum chewing, and after abstaining from both smoking and gum chewing. After a median of 11 weeks of chewing nicotine gum, 52 persons (43%) remained abstinent from smoking and chewing for at least 12 weeks. In these successful study participants, low-density lipoprotein (LDL)-cholesterol levels decreased significantly by a mean of 7.5 mg/dL (5.6%). High-density lipoprotein (HDL)-cholesterol increased by 5 to 6 mg/dL during the first weeks after ceasing to smoke, but levels at the end of study were only 2.1 mg/dL (3.4%) higher than baseline (nonsignificant difference). Triglyceride levels did not change during smoking cessation. While systolic blood pressure remained unchanged, diastolic blood pressure increased significantly by a mean of 3.5 mm Hg. For LDL-cholesterol, HDL-cholesterol, and systolic and diastolic blood pressure, there was an inverse correlation between the respective baseline values and the observed changes during the cessation of smoking. The urinary excretion of adrenaline and noradrenaline decreased upon quitting. The volume of platelets became significantly less during smoking cessation, but aggregation induced by adenosine diphosphate (ADP) and collagen and thromboxane synthesis in vitro remained uninfluenced. The platelet cyclic adenosine monophosphate (cAMP) response to stimulation of adenylate cyclase with prostaglandin E1 showed marked enhancement upon quitting. The changes observed intraindividually during smoking cessation largely correspond to the differences between smokers and nonsmokers described in epidemiologic studies. For serum lipids and blood pressure, a significant dependence of the changes on the respective values at baseline may indicate greater benefit for persons at higher risk. Decreased platelet volume and increased susceptibility of platelets to antiaggregatory prostaglandin E1 indicate a favorable influence of quitting on platelet reactivity.

Adult↗
PubMed1993

Evidence for sustained platelet activation in patients with early postinfarction angina.

Excretion of 2,3-dinor-thromboxane B2 released from activated platelets has been found elevated in patients with acute myocardial infarction and unstable angina. To investigate the role of thrombotic activity in postinfarction angina we measured urinary concentrations of 2,3-dinorthromboxane B2 in 20 patients over 10 days after myocardial infarction. Compared with 11 patients recovering pain-free, excretion of 2,3-dinorthromboxane B2 was found elevated in 9 patients who developed postinfarction angina. Accordingly, early postinfarction angina appears to be associated with ongoing thrombotic activity.

Aged↗
PubMed1993

Effects of lipoprotein(a) on in vitro lysis of whole blood thrombi from healthy volunteers.

Elevated levels of lipoprotein(a) [Lp(a)] were shown to be an independent cardiovascular risk factor. Structural homologies between Lp(a) and plasminogen could be of importance for this. In the present study, the influence of Lp(a) on in vitro lysis of thrombi produced in recalcified whole blood was investigated. Of 120 healthy volunteers, 21 (18%) had serum Lp(a) levels > or = 25 mg/dl (median 70 mg/dl). Compared to 46 controls with serum Lp(a) < 25 mg/dl (median 7 mg/dl), the weight of whole blood thrombi generated in vitro was similar (96 +/- 11 vs. 94 +/- 13 mg). Thrombolysis with exogenously added tissue plasminogen activator (TPA; 0.1, 0.4 and 1.6 mg/l) was not affected by the ex vivo concentration of Lp(a). In persons with elevated Lp(a), plasma TPA levels were higher than in persons with low Lp(a) [15.7 +/- 1.5 vs. 11.7 +/- 1.2 micrograms/l; p = 0.051], but plasminogen activator inhibitor (PAI) activity and the plasma concentrations of PAI-1 were also higher. When Lp(a) was added in vitro to blood with low baseline Lp(a) [median final concentration 47 mg/dl], thrombolysis was significantly inhibited with low doses of TPA (0.1 and 0.4 mg/l), but remained unaffected with TPA 1.6 mg/l. Thus, the inhibitory effect of Lp(a) on thrombolysis seems to be counterregulated in blood of healthy volunteers with elevated Lp(a).

Adult↗